{"title":"miR-21-5p 靶向 PIK3R1 调控 NF-κB 信号通路,抑制泌乳素瘤的侵袭和进展","authors":"Min de Li, Juan Yang, Xiao Wu, Shang Si Chen","doi":"10.1155/ije/7741091","DOIUrl":null,"url":null,"abstract":"<p><p>Prolactinomas (PRLs) are benign tumors with malignant characteristics that can invade the surrounding tissue structures and are challenging to treat. It has been reported that miR-21-5p expression in pituitary adenomas is correlated with tumor invasion and size. However, the mechanism of action of miR-21-5p in PRL remains unclear. Dysregulation of the phosphoinositide-3-kinase (PI3K) regulatory Subunit 1 pathway occurs frequently in cancer and plays an important role in tumor progression as an important component of the PI3K pathway. However, the role of PIK3R1 in PRL and its regulatory mechanism are unknown. In this study, we first explored the effect of miR-21-5p in PRL and then confirmed that PIK3R1 is a direct target of miR-21-5p using bioinformatics and cellular experiments. Subsequent in vitro experiments demonstrated that overexpression of PIK3R1 significantly attenuated the biological effects of miR-21-5p in PRL cells, such as promoting proliferation and invasion. Finally, we explored the mechanism by which PIK3R1 affects PRL progression and found that the inhibition of I<i>κ</i>Ba degradation by PIK3R1 impacts PRL progression via the miR-21-5p/PIK3R1/MMP pathway.</p>","PeriodicalId":13966,"journal":{"name":"International Journal of Endocrinology","volume":"2025 ","pages":"7741091"},"PeriodicalIF":2.3000,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11824381/pdf/","citationCount":"0","resultStr":"{\"title\":\"miR-21-5p Targets PIK3R1 to Regulate the NF-<i>κ</i>B Signaling Pathway, Inhibiting the Invasion and Progression of Prolactinoma.\",\"authors\":\"Min de Li, Juan Yang, Xiao Wu, Shang Si Chen\",\"doi\":\"10.1155/ije/7741091\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Prolactinomas (PRLs) are benign tumors with malignant characteristics that can invade the surrounding tissue structures and are challenging to treat. It has been reported that miR-21-5p expression in pituitary adenomas is correlated with tumor invasion and size. However, the mechanism of action of miR-21-5p in PRL remains unclear. Dysregulation of the phosphoinositide-3-kinase (PI3K) regulatory Subunit 1 pathway occurs frequently in cancer and plays an important role in tumor progression as an important component of the PI3K pathway. However, the role of PIK3R1 in PRL and its regulatory mechanism are unknown. In this study, we first explored the effect of miR-21-5p in PRL and then confirmed that PIK3R1 is a direct target of miR-21-5p using bioinformatics and cellular experiments. Subsequent in vitro experiments demonstrated that overexpression of PIK3R1 significantly attenuated the biological effects of miR-21-5p in PRL cells, such as promoting proliferation and invasion. Finally, we explored the mechanism by which PIK3R1 affects PRL progression and found that the inhibition of I<i>κ</i>Ba degradation by PIK3R1 impacts PRL progression via the miR-21-5p/PIK3R1/MMP pathway.</p>\",\"PeriodicalId\":13966,\"journal\":{\"name\":\"International Journal of Endocrinology\",\"volume\":\"2025 \",\"pages\":\"7741091\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2025-02-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11824381/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Endocrinology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1155/ije/7741091\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Endocrinology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1155/ije/7741091","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
miR-21-5p Targets PIK3R1 to Regulate the NF-κB Signaling Pathway, Inhibiting the Invasion and Progression of Prolactinoma.
Prolactinomas (PRLs) are benign tumors with malignant characteristics that can invade the surrounding tissue structures and are challenging to treat. It has been reported that miR-21-5p expression in pituitary adenomas is correlated with tumor invasion and size. However, the mechanism of action of miR-21-5p in PRL remains unclear. Dysregulation of the phosphoinositide-3-kinase (PI3K) regulatory Subunit 1 pathway occurs frequently in cancer and plays an important role in tumor progression as an important component of the PI3K pathway. However, the role of PIK3R1 in PRL and its regulatory mechanism are unknown. In this study, we first explored the effect of miR-21-5p in PRL and then confirmed that PIK3R1 is a direct target of miR-21-5p using bioinformatics and cellular experiments. Subsequent in vitro experiments demonstrated that overexpression of PIK3R1 significantly attenuated the biological effects of miR-21-5p in PRL cells, such as promoting proliferation and invasion. Finally, we explored the mechanism by which PIK3R1 affects PRL progression and found that the inhibition of IκBa degradation by PIK3R1 impacts PRL progression via the miR-21-5p/PIK3R1/MMP pathway.
期刊介绍:
International Journal of Endocrinology is a peer-reviewed, Open Access journal that provides a forum for scientists and clinicians working in basic and translational research. The journal publishes original research articles, review articles, and clinical studies that provide insights into the endocrine system and its associated diseases at a genomic, molecular, biochemical and cellular level.